Selective oxidation and externalization of membrane phosphatidylserine: Bcl-2-induced potentiation of the final common pathway for apoptosis

Brain Res. 1999 Jun 12;831(1-2):125-30. doi: 10.1016/s0006-8993(99)01414-6.

Abstract

The induction of apoptosis in PC12 cells by the enediyne neocarzinostatin (NCS) is paradoxically potentiated by overexpression of bcl-2. The enhanced activation of NCS seen in bcl-2-overexpressing cells cannot by itself be responsible for the potentiation of apoptosis, since Bcl-2 would be expected to block apoptosis at a point distal to NCS activation (e.g., in the apoptosis final common pathway). We now report that overexpression of bcl-2 in PC12 cells does not protect the cells from NCS-induced oxidation of membrane phosphatidylserine (PS), and results in potentiation of NCS-induced externalization of membrane PS, two events associated with the apoptosis final common pathway. The mechanism of potentiation of apoptosis by Bcl-2 is related to the enhanced reducing potential of bcl-2-overexpressing PC12 cells.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Apoptosis / physiology*
  • Gene Expression Regulation / physiology*
  • Genes, bcl-2*
  • Lipid Peroxidation / physiology*
  • Membranes / metabolism
  • Oxidation-Reduction
  • PC12 Cells
  • Phosphatidylserines / metabolism*
  • Rats
  • Transfection
  • Zinostatin / pharmacology

Substances

  • Phosphatidylserines
  • Zinostatin